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Article ; Online: The Effects of Vitamin D on Immune System and Inflammatory Diseases.

Ao, Tomoka / Kikuta, Junichi / Ishii, Masaru

2021 Volume 11, Issue 11

Abstract: Immune cells, including dendritic cells, macrophages, and T and B cells, express the vitamin D receptor and 1α-hydroxylase. In vitro studies have shown that 1,25-dihydroxyvitamin D, the active form of vitamin D, has an anti-inflammatory effect. Recent ... ...

Abstract	Immune cells, including dendritic cells, macrophages, and T and B cells, express the vitamin D receptor and 1α-hydroxylase. In vitro studies have shown that 1,25-dihydroxyvitamin D, the active form of vitamin D, has an anti-inflammatory effect. Recent epidemiological evidence has indicated a significant association between vitamin D deficiency and an increased incidence, or aggravation, of infectious diseases and inflammatory autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis. However, the impact of vitamin D on treatment and prevention, particularly in infectious diseases such as the 2019 coronavirus disease (COVID-19), remains controversial. Here, we review recent evidence associated with the relationship between vitamin D and inflammatory diseases and describe the underlying immunomodulatory effect of vitamin D.
MeSH term(s)	Animals ; Arthritis, Rheumatoid/drug therapy ; Arthritis, Rheumatoid/prevention & control ; Autoimmune Diseases/drug therapy ; B-Lymphocytes/immunology ; COVID-19/drug therapy ; COVID-19/prevention & control ; Dendritic Cells/immunology ; Disease Models, Animal ; Humans ; Immune System/drug effects ; Inflammation/drug therapy ; Influenza, Human/drug therapy ; Influenza, Human/prevention & control ; Lupus Erythematosus, Systemic/drug therapy ; Lupus Erythematosus, Systemic/prevention & control ; Macrophages/immunology ; Mice ; Monocytes/immunology ; Multiple Sclerosis/drug therapy ; Multiple Sclerosis/prevention & control ; Receptors, Calcitriol/genetics ; Receptors, Calcitriol/physiology ; T-Lymphocytes/immunology ; Vitamin D/therapeutic use ; Vitamin D Deficiency/complications
Chemical Substances	Receptors, Calcitriol ; VDR protein, human ; Vitamin D (1406-16-2)
Language	English
Publishing date	2021-11-03
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom11111624
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Two Cases of Gouty Sacroiliitis Evaluated by Dual-energy Computed Tomography.

Ao, Tomoka / Shoda, Hirofumi / Yamamoto, Kazuhiko

The Journal of rheumatology

2016 Volume 43, Issue 6, Page(s) 1146–1147

Language	English
Publishing date	2016-06
Publishing country	Canada
Document type	Journal Article
ZDB-ID	194928-7
ISSN	1499-2752 ; 0315-162X
ISSN (online)	1499-2752
ISSN	0315-162X
DOI	10.3899/jrheum.151454
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Zs.A 1168: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 135: Show issues

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Article: [Update on recent progress in vitamin D research. The effects of vitamin D in autoinflammatory diseases.]

Ao, Tomoka / Kikuta, Junichi / Ishii, Masaru

Clinical calcium

2017 Volume 27, Issue 11, Page(s) 1551–1559

Abstract: Various kinds of immune cells -including dendritic cells, macrophages, T cells and B cells- express the vitamin D receptor and 1α-hydroxylase(CYP27B1). ...

Abstract	Various kinds of immune cells -including dendritic cells, macrophages, T cells and B cells- express the vitamin D receptor and 1α-hydroxylase(CYP27B1).
Language	Japanese
Publishing date	2017
Publishing country	Japan
Document type	English Abstract ; Journal Article
ZDB-ID	2386417-5
ISSN	0917-5857
ISSN	0917-5857
DOI	CliCa171115511559
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Zs.A 6536: Show issues

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Article ; Online: Local sympathetic neurons promote neutrophil egress from the bone marrow at the onset of acute inflammation.

Ao, Tomoka / Kikuta, Junichi / Sudo, Takao / Uchida, Yutaka / Kobayashi, Kenta / Ishii, Masaru

International immunology

2020 Volume 32, Issue 11, Page(s) 727–736

Abstract: The sympathetic nervous system plays critical roles in the differentiation, maturation and recruitment of immune cells under homeostatic conditions, and in responses to environmental stimuli, although its role in the migratory control of immune cells ... ...

Abstract	The sympathetic nervous system plays critical roles in the differentiation, maturation and recruitment of immune cells under homeostatic conditions, and in responses to environmental stimuli, although its role in the migratory control of immune cells during acute inflammation remains unclear. In this study, using an advanced intravital bone imaging system established in our laboratory, we demonstrated that the sympathetic nervous system locally regulates neutrophil egress from the bone marrow for mobilization to inflammatory foci. We found that sympathetic neurons were located close to blood vessels in the bone marrow cavity; moreover, upon lipopolysaccharide (LPS) administration, local sympathectomy delayed neutrophil egress from the bone marrow and increased the proportion of neutrophils that remained in place. We also showed that vascular endothelial cells produced C-X-C motif chemokine ligand 1 (CXCL1), which is responsible for neutrophil egress out of the bone marrow. Its expression was up-regulated during acute inflammation, and was suppressed by β-adrenergic receptor blockade, which was accompanied with inhibition of neutrophil egress into the systemic circulation. Furthermore, systemic β-adrenergic signaling blockade decreased the recruitment of neutrophils in the lung under conditions of acute systemic inflammation. Taken together, the results of this study first suggested a new regulatory system, wherein local sympathetic nervous activation promoted neutrophil egress by enhancing Cxcl1 expression in bone marrow endothelial cells in a β-adrenergic signaling-dependent manner, contributing to the recruitment of neutrophils at the onset of inflammation in vivo.
MeSH term(s)	Animals ; Bone Marrow/immunology ; Inflammation/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Neurons/immunology ; Neutrophils/immunology
Language	English
Publishing date	2020-04-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1013745-2
ISSN	1460-2377 ; 0953-8178
ISSN (online)	1460-2377
ISSN	0953-8178
DOI	10.1093/intimm/dxaa025
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Zs.A 2619: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 70: Show issues

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Article ; Online: Anti-Siglec-15 antibody suppresses bone resorption by inhibiting osteoclast multinucleation without attenuating bone formation.

Tsukazaki, Hiroyuki / Kikuta, Junichi / Ao, Tomoka / Morimoto, Akito / Fukuda, Chie / Tsuda, Eisuke / Minoshima, Masafumi / Kikuchi, Kazuya / Kaito, Takashi / Ishii, Masaru

Bone

2021 Volume 152, Page(s) 116095

Abstract: Anti-resorptive drugs are widely used for the treatment of osteoporosis, but excessive inhibition of osteoclastogenesis can suppress bone turnover and cause the deterioration of bone quality. Sialic acid-binding immunoglobulin-like lectin 15 (Siglec-15) ... ...

Abstract	Anti-resorptive drugs are widely used for the treatment of osteoporosis, but excessive inhibition of osteoclastogenesis can suppress bone turnover and cause the deterioration of bone quality. Sialic acid-binding immunoglobulin-like lectin 15 (Siglec-15) is a transmembrane protein expressed on osteoclast precursor cells and mature osteoclasts. Siglec-15 regulates proteins containing immunoreceptor tyrosine-based activation motif (ITAM) domains, which then induce nuclear factor of activated T-cells 1 (NFATc1), a master transcription factor of osteoclast differentiation. Anti-Siglec-15 antibody modulates ITAM signaling in osteoclast precursors and inhibits the maturation of osteoclasts in vitro. However, in situ pharmacological effects, particularly during postmenopausal osteoporosis, remain unclear. Here, we demonstrated that anti-Siglec-15 antibody treatment protected against ovariectomy-induced bone loss by specifically inhibiting the generation of multinucleated osteoclasts in vivo. Moreover, treatment with anti-Siglec-15 antibody maintained bone formation to a greater extent than with risedronate, the first-line treatment for osteoporosis. Intravital imaging revealed that anti-Siglec-15 antibody treatment did not cause a reduction in osteoclast motility, whereas osteoclast motility declined following risedronate treatment. We evaluated osteoclast activity using a pH-sensing probe and found that the bone resorptive ability of osteoclasts was lower following anti-Siglec-15 antibody treatment compared to after risedronate treatment. Our findings suggest that anti-Siglec-15 treatment may have potential as an anti-resorptive therapy for osteoporosis, which substantially inhibits the activity of osteoclasts while maintaining physiological bone coupling.
MeSH term(s)	Bone Resorption/drug therapy ; Bone and Bones ; Cell Differentiation ; Female ; Humans ; NFATC Transcription Factors ; Osteoclasts ; Osteogenesis ; RANK Ligand
Chemical Substances	NFATC Transcription Factors ; RANK Ligand
Language	English
Publishing date	2021-07-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	632515-4
ISSN	1873-2763 ; 8756-3282
ISSN (online)	1873-2763
ISSN	8756-3282
DOI	10.1016/j.bone.2021.116095
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Zs.A 1571: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 332: Show issues

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Article ; Online: Osteoblast-derived vesicles induce a switch from bone-formation to bone-resorption in vivo

Maki Uenaka / Erika Yamashita / Junichi Kikuta / Akito Morimoto / Tomoka Ao / Hiroki Mizuno / Masayuki Furuya / Tetsuo Hasegawa / Hiroyuki Tsukazaki / Takao Sudo / Keizo Nishikawa / Daisuke Okuzaki / Daisuke Motooka / Nobuyoshi Kosaka / Fuminori Sugihara / Thomas Boettger / Thomas Braun / Takahiro Ochiya / Masaru Ishii

Nature Communications, Vol 13, Iss 1, Pp 1-

2022 Volume 13

Abstract: Bone remodeling involves a switch between bone formation and resorption, but the mechanisms is unclear. Here, the authors show that intercellular communication via extracellular vesicles secreted by mature osteoblasts is a key factor for the switching, ... ...

Abstract	Bone remodeling involves a switch between bone formation and resorption, but the mechanisms is unclear. Here, the authors show that intercellular communication via extracellular vesicles secreted by mature osteoblasts is a key factor for the switching, via a microRNA-mediated mechanism.
Keywords	Science ; Q
Language	English
Publishing date	2022-02-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Thrombomodulin induces anti-inflammatory effects by inhibiting the rolling adhesion of leukocytes in vivo.

Nishizawa, Shino / Kikuta, Junichi / Seno, Shigeto / Kajiki, Masahiro / Tsujita, Ryuichi / Mizuno, Hiroki / Sudo, Takao / Ao, Tomoka / Matsuda, Hideo / Ishii, Masaru

Journal of pharmacological sciences

2020 Volume 143, Issue 1, Page(s) 17–22

Abstract: Thrombomodulin (TM) is an integral membrane protein expressed on the surface of vascular endothelial cells that suppresses blood coagulation. Recent studies have shown that TM exhibits anti-inflammatory effects by inhibiting leukocyte recruitment. ... ...

Abstract	Thrombomodulin (TM) is an integral membrane protein expressed on the surface of vascular endothelial cells that suppresses blood coagulation. Recent studies have shown that TM exhibits anti-inflammatory effects by inhibiting leukocyte recruitment. However, the actual modes of action of TM in vivo remain unclear. Here, we describe the pharmacological effects of recombinant human soluble TM (TM alfa) on leukocyte dynamics in living mice using intravital imaging techniques. Under control conditions, neutrophils exhibited three distinct types of adhesion behavior in vessels: 1) "non-adhesion", in which cells flowed without vessel adhesion; 2) "rolling adhesion", in which cells transiently interacted with the endothelium; and 3) "tight binding", in which cells bound strongly to the endothelial cells. Compared to control conditions, local lipopolysaccharide stimulation resulted in an increased frequency of rolling adhesion that was not homogeneously distributed on vessel walls but occurred at specific endothelial sites. Under inflammatory conditions, TM alfa, particularly the D1 domain which is a lectin-like region of TM, significantly decreased the frequency of rolling adhesion, but did not influence the number of tight bindings. This was the first study to demonstrate that TM alfa exerts anti-inflammatory effects by inhibiting rolling adhesion of neutrophils to vascular endothelial cells in living mice.
MeSH term(s)	Animals ; Anti-Inflammatory Agents ; Cell Adhesion ; Endothelium, Vascular/cytology ; Male ; Mice, Inbred C57BL ; Molecular Imaging/methods ; Neutrophils/physiology ; Recombinant Proteins/pharmacology ; Thrombomodulin/physiology
Chemical Substances	Anti-Inflammatory Agents ; Recombinant Proteins ; Thrombomodulin
Language	English
Publishing date	2020-01-14
Publishing country	Japan
Document type	Journal Article
ZDB-ID	2104264-0
ISSN	1347-8648 ; 1347-8613
ISSN (online)	1347-8648
ISSN	1347-8613
DOI	10.1016/j.jphs.2020.01.001
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Article ; Online: Osteoblast-derived vesicles induce a switch from bone-formation to bone-resorption in vivo.

Uenaka, Maki / Yamashita, Erika / Kikuta, Junichi / Morimoto, Akito / Ao, Tomoka / Mizuno, Hiroki / Furuya, Masayuki / Hasegawa, Tetsuo / Tsukazaki, Hiroyuki / Sudo, Takao / Nishikawa, Keizo / Okuzaki, Daisuke / Motooka, Daisuke / Kosaka, Nobuyoshi / Sugihara, Fuminori / Boettger, Thomas / Braun, Thomas / Ochiya, Takahiro / Ishii, Masaru

Nature communications

2022 Volume 13, Issue 1, Page(s) 1066

Abstract: Bone metabolism is regulated by the cooperative activity between bone-forming osteoblasts and bone-resorbing osteoclasts. However, the mechanisms mediating the switch between the osteoblastic and osteoclastic phases have not been fully elucidated. Here, ... ...

Abstract	Bone metabolism is regulated by the cooperative activity between bone-forming osteoblasts and bone-resorbing osteoclasts. However, the mechanisms mediating the switch between the osteoblastic and osteoclastic phases have not been fully elucidated. Here, we identify a specific subset of mature osteoblast-derived extracellular vesicles that inhibit bone formation and enhance osteoclastogenesis. Intravital imaging reveals that mature osteoblasts secrete and capture extracellular vesicles, referred to as small osteoblast vesicles (SOVs). Co-culture experiments demonstrate that SOVs suppress osteoblast differentiation and enhance the expression of receptor activator of NF-κB ligand, thereby inducing osteoclast differentiation. We also elucidate that the SOV-enriched microRNA miR-143 inhibits Runt-related transcription factor 2, a master regulator of osteoblastogenesis, by targeting the mRNA expression of its dimerization partner, core-binding factor β. In summary, we identify SOVs as a mode of cell-to-cell communication, controlling the dynamic transition from bone-forming to bone-resorbing phases in vivo.
MeSH term(s)	Bone Resorption/metabolism ; Cell Differentiation ; Humans ; Osteoblasts/metabolism ; Osteoclasts/metabolism ; Osteogenesis/genetics ; RANK Ligand/metabolism ; Signal Transduction
Chemical Substances	RANK Ligand
Language	English
Publishing date	2022-02-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-28673-2
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Article ; Online: Group 2 innate lymphoid cells support hematopoietic recovery under stress conditions.

Sudo, Takao / Motomura, Yasutaka / Okuzaki, Daisuke / Hasegawa, Tetsuo / Yokota, Takafumi / Kikuta, Junichi / Ao, Tomoka / Mizuno, Hiroki / Matsui, Takahiro / Motooka, Daisuke / Yoshizawa, Ryosuke / Nagasawa, Takashi / Kanakura, Yuzuru / Moro, Kazuyo / Ishii, Masaru

The Journal of experimental medicine

2021 Volume 218, Issue 5

Abstract: The cell-cycle status of hematopoietic stem and progenitor cells (HSPCs) becomes activated following chemotherapy-induced stress, promoting bone marrow (BM) regeneration; however, the underlying molecular mechanism remains elusive. Here we show that BM- ... ...

Abstract	The cell-cycle status of hematopoietic stem and progenitor cells (HSPCs) becomes activated following chemotherapy-induced stress, promoting bone marrow (BM) regeneration; however, the underlying molecular mechanism remains elusive. Here we show that BM-resident group 2 innate lymphoid cells (ILC2s) support the recovery of HSPCs from 5-fluorouracil (5-FU)-induced stress by secreting granulocyte-macrophage colony-stimulating factor (GM-CSF). Mechanistically, IL-33 released from chemo-sensitive B cell progenitors activates MyD88-mediated secretion of GM-CSF in ILC2, suggesting the existence of a B cell-ILC2 axis for maintaining hematopoietic homeostasis. GM-CSF knockout mice treated with 5-FU showed severe loss of myeloid lineage cells, causing lethality, which was rescued by transferring BM ILC2s from wild-type mice. Further, the adoptive transfer of ILC2s to 5-FU-treated mice accelerates hematopoietic recovery, while the reduction of ILC2s results in the opposite effect. Thus, ILC2s may function by "sensing" the damaged BM spaces and subsequently support hematopoietic recovery under stress conditions.
MeSH term(s)	Animals ; Bone Marrow/drug effects ; Bone Marrow/metabolism ; Bone Marrow Cells/cytology ; Bone Marrow Cells/drug effects ; Bone Marrow Cells/metabolism ; Cells, Cultured ; Fluorouracil/pharmacology ; Gene Expression Profiling/methods ; Granulocyte-Macrophage Colony-Stimulating Factor/genetics ; Granulocyte-Macrophage Colony-Stimulating Factor/metabolism ; Hematopoietic Stem Cell Transplantation/methods ; Hematopoietic Stem Cells/cytology ; Hematopoietic Stem Cells/drug effects ; Hematopoietic Stem Cells/metabolism ; Immunity, Innate/drug effects ; Immunity, Innate/immunology ; Immunosuppressive Agents/pharmacology ; Lymphocytes/drug effects ; Lymphocytes/immunology ; Lymphocytes/metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Microscopy, Confocal ; Reverse Transcriptase Polymerase Chain Reaction ; Mice
Chemical Substances	Immunosuppressive Agents ; Granulocyte-Macrophage Colony-Stimulating Factor (83869-56-1) ; Fluorouracil (U3P01618RT)
Language	English
Publishing date	2021-03-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20200817
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Ua VI Zs.107: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 45: Show issues

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Article ; Online: PGE2 induced in and released by dying cells functions as an inhibitory DAMP.

Hangai, Sho / Ao, Tomoka / Kimura, Yoshitaka / Matsuki, Kosuke / Kawamura, Takeshi / Negishi, Hideo / Nishio, Junko / Kodama, Tatsuhiko / Taniguchi, Tadatsugu / Yanai, Hideyuki

Proceedings of the National Academy of Sciences of the United States of America

2016 Volume 113, Issue 14, Page(s) 3844–3849

Abstract: Cellular components released into the external milieu as a result of cell death and sensed by the body are generally termed damage-associated molecular patterns (DAMPs). Although DAMPs are conventionally thought to be protective to the host by evoking ... ...

Abstract	Cellular components released into the external milieu as a result of cell death and sensed by the body are generally termed damage-associated molecular patterns (DAMPs). Although DAMPs are conventionally thought to be protective to the host by evoking inflammatory responses important for immunity and wound repair, there is the prevailing notion that dysregulated release of DAMPs can also underlie or exacerbate disease development. However, the critical issue for how resultant DAMP-mediated responses are regulated has heretofore not been fully addressed. In the present study, we identify prostaglandin E2 (PGE2) as a DAMP that negatively regulates immune responses. We show that the production of PGE2 is augmented under cell death-inducing conditions via the transcriptional induction of the cyclooxygenase 2 (COX2) gene and that cell-released PGE2 suppresses the expression of genes associated with inflammation, thereby limiting the cell's immunostimulatory activities. Consistent with this, inhibition of the PGE2 synthesis pathway potentiates the inflammation induced by dying cells. We also provide in vivo evidence for a protective role of PGE2 released upon acetaminophen-induced liver injury as well as a pathogenic role for PGE2 during tumor cell growth. Our study places this classically known lipid mediator in an unprecedented context-that is, an inhibitory DAMP vis-à-vis activating DAMPs, which may have translational implications for designing more effective therapeutic regimens for inflammation-associated diseases.
MeSH term(s)	Acetaminophen/adverse effects ; Alarmins/metabolism ; Animals ; Cell Death/immunology ; Cell Death/physiology ; Cell Line, Tumor ; Chemical and Drug Induced Liver Injury/immunology ; Cyclooxygenase 2/biosynthesis ; Dinoprostone/metabolism ; HeLa Cells ; Humans ; Inflammation/immunology ; Inflammation/pathology ; Lipopolysaccharides ; Mice ; Mice, Inbred C57BL
Chemical Substances	Alarmins ; Lipopolysaccharides ; Acetaminophen (362O9ITL9D) ; Ptgs2 protein, mouse (EC 1.14.99.-) ; Cyclooxygenase 2 (EC 1.14.99.1) ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2016-04-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1602023113
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